A5091004058- Renal Diseases and Glomerulopathies
- Systemic Lupus Erythematosus Research
- Immune Response and Inflammation
- Inflammasome and immune disorders
- Chronic Kidney Disease and Diabetes
- Chemokine receptors and signaling
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Immune cells in cancer
- T-cell and B-cell Immunology
- Immune Cell Function and Interaction
- Renal and related cancers
- Acute Kidney Injury Research
- Phagocytosis and Immune Regulation
- Cell Adhesion Molecules Research
- Vasculitis and related conditions
- Gout, Hyperuricemia, Uric Acid
- Atherosclerosis and Cardiovascular Diseases
- interferon and immune responses
- Immunotherapy and Immune Responses
- Cytokine Signaling Pathways and Interactions
- Cancer Research and Treatments
- Kidney Stones and Urolithiasis Treatments
- IL-33, ST2, and ILC Pathways
- Diabetes Treatment and Management
- Dialysis and Renal Disease Management
Ludwig-Maximilians-Universität München
2016-2025
LMU Klinikum
2016-2025
Angiologica (Italy)
2024
Institut für Urheber- und Medienrecht
2024
Metabolism and Renal Physiology
2024
RELX Group (United States)
2016-2023
Meyer Children's Hospital
2023
Karolinska Institutet
2023
Washington University in St. Louis
2023
Novartis (France)
2023
Significance Cell death by regulated necrosis causes tremendous tissue damage in a wide variety of diseases, including myocardial infarction, stroke, sepsis, and ischemia–reperfusion injury upon solid organ transplantation. Here, we demonstrate that an iron-dependent form necrosis, referred to as ferroptosis, mediates synchronized functional units diverse organs ischemia other stimuli, thereby triggering detrimental immune response. We developed novel third-generation inhibitor ferroptosis...
Objective To update the 2012 EULAR/ERA–EDTA recommendations for management of lupus nephritis (LN). Methods Following EULAR standardised operating procedures, a systematic literature review was performed. Members multidisciplinary Task Force voted independently on their level agreeement with formed statements. Results The changes include treatment targets, use glucocorticoids and calcineurin inhibitors (CNIs) end-stage kidney disease (ESKD). target therapy is complete response (proteinuria...
Abstract The chemokine receptors CCR2 and CCR5 play important roles in the recruitment of monocytes/macrophages T cells. To better understand role both murine models inflammatory diseases to recognize potential problems when correlating these data humans, we have generated mAbs against CCR5. In mice is homogeneously expressed on monocytes 2–15% cells, closely resembling expression pattern humans. contrast NK cells are highly positive. addition, 3–10% CD4 10–40% CD8-positive weakly detectable...
Nephrocalcinosis, acute calcium oxalate (CaOx) nephropathy, and renal stone disease can lead to inflammation subsequent failure, but the underlying pathological mechanisms remain elusive. Other crystallopathies, such as gout, atherosclerosis, asbestosis, trigger tissue remodeling by inducing IL-1β secretion, leading us hypothesize that CaOx crystals may induce in a similar manner. In mice, intrarenal deposition induced tubular damage, cytokine expression, neutrophil recruitment, failure. We...
In AKI, dying renal cells release intracellular molecules that stimulate immune to secrete proinflammatory cytokines, which trigger leukocyte recruitment and inflammation. Whether the of histones, specifically, from contributes inflammation AKI is unknown. this study, we found tubular epithelial released histones into extracellular space, directly interacted with Toll-like receptor (TLR)-2 (TLR2) TLR4 induce MyD88, NF-κB, mitogen activated protein kinase signaling. Extracellular also had...
Severe AKI is often associated with multiorgan dysfunction, but the mechanisms of this remote tissue injury are unknown. We hypothesized that renal necroinflammation releases cytotoxic molecules may cause organ damage. In hypoxia-induced tubular epithelial cell necrosis in vitro, histone secretion from ischemic cells primed neutrophils to form neutrophil extracellular traps. These traps induced death and stimulated trap formation fresh neutrophils. vivo, ischemia-reperfusion mouse kidney...